Urban living, industrial employment and cigarette smoking bring man into daily contact with carbon monoxide (CO). It is known that prolonged sublethal CO poisoning can lead to polycythemia and cardiac enlargement. However, the detailed morphologic effects and physiologic, metabolic and enzymic effects on heart are poorly understood. We intend to investigate the effects of chronic CO exposure (500 p.p.m. for 30 days) on the following parameters in rat heart; a. Morphologic changes in left ventricle, right ventricle and atria, b. Tolerance to anoxia by the heart in the intact animal, c. Tolerance to anoxia of the left ventricle, right ventricle and atria in isolated preparations, d. Aerobic levels of creatine phosphate, ATP, ADP. AMP and Pi and changes following short periods of anoxia, e. Glycolytic capacity of the whole isolated perfused heart, f. Glycogen levels and extent of glycogen depletion following anoxic exposure, g. Activities of the rate limiting glycolytic enzymes hexokinase, phosphofructokinase, glyceraldehydephosphate dehydrogenase and pyruvate kinase, h. Lactate dehydrogenase activity and isozyme patterns in left ventricle, right ventricle and atria. The studies outlined in this proposal will provide mammalian myocardium as a result of prolonged exposure about in the normal mammalian myocardium as a result of prolonged exposure to CO. They should also provide information basic to designs of future studies dealing with, a. Interaction of CO effects with various cardiac and respiratory problems (i.e. coronary artery disease, congestive heart failure, emphysema, etc.), b. Determination of threshold limits for cardiac effects following long-term CO exposure. The initiation and success of such studies will of necessity depend on the completion of the studies outlined in the present proposal.